Antibodies may further damage spinal cord injuries
In the Journal of Clinical Investigation has found that white blood cells actually damage more structures in the spine around the area of original damage. The Ohio State University Study further showed that the damage caused by antibodies could help to explain why patients that have spinal cord injuries lose functionality over time. The study further recommends that drugs that inhibit antibodies may help those with a spinal cord injury to keep their present level of functionality, but did not elaborate on levels or how to deal with sickness tied to the immunosupression drugs. The problem with antibodies was found while work was done in studies of rats that had spinal cord injuries. Over time they began to lose strength and mobility but did not have any disease or bacteria to answer why this was happening. After further study they found that antibodies were damaging nerves and other structures in the spine. (Source: EurekAlert)
This is something that we all should discuss with our doctors. Depending on the type of injury you have, it may be worthwhile to check and see if your immune system is causing additional damage to the spine. Up to this point, it as a mystery why things seemed to degrade over time. No one knew if this was a brain issue, spinal problems or muscle atrophy. Now we know that our own immune system is making mistakes and is damaging rather than helping to repair areas in the spine. It will be interesting if ties can be made to auto-immune diseases and whether this has some kind of relationship with them. No one wants to lose any functionality and if we have a way to keep this damage from happening, we can help to increase quality of life. A study should be done where drugs that are used for auto-immune diseases are given to spinal cord injury patients over time and see if they have more functionality than those who were not given those drugs.
If you enjoyed this post, please consider to leave a comment or subscribe to the feed and get future articles delivered to your feed reader.
Loading ...
User Comments
No comments yet.
Sorry, the comment form is closed at this time.